An analysis of RNA-containing virus-specific structures was performed in the course of the establishment of persistent infection with SV5 virus in L cells. It was observed that up to the 11th passage in the LSV5 system, the same virus-specific structures were synthesized as in acute infection. At the level of the 18th passage synthesis of intracellular RNP was reduced and high 3H-uridine incorporation into light structures was observed. In the last passages examined (25th and 31st), the structures with rho 1.18--1.17 g/ml were predominant. The sedimentation RNA analysis (the 3rd, 6th, and 11th passages) revealed 50 S, 35--32 S, 24 S, and 18 S RNA. At later passages (25th and 31st), synthesis of 35 S, 24--22 S and lighter RNAs was dominant. The possibility of relationship between reduced 50 S RNA synthesis and low infectivity of intracellular virus is discussed.

Animals↗

PubMedDate not supplied

[Persistence of Newcastle disease virus in mouse cells].

The course of persistent infection in Newcastle disease virus (NDV)-infected mouse L cells (LNDV) was analysed. The production of infectious intra- and extracellular virus was markedly reduced (less than 10(1) PFU/ml), 30% of the cells produced virus-specific antigen. Analysis of the synthesis of 3H-nucleocapsid RNA in the LNDV system revealed predominance of low molecular weight RNAs. Virus-specific sequences were shown to be present in fraction of DNA extracted by Hirt's method. Only the "supernatant" Hirt's fraction was infectious. The possibility of the presence of virus-specific sequences in free unintegrated form is discussed.

Animals↗

PubMedDate not supplied

[Comparison of double triple integration systems].

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Cell Line↗

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[Persistent infection in murine L cells infected with the parainfluenza virus SV5].

Persistent infection of mouse L cells was achieved by serial passages of undiluted parainfluenza SV5 virus. At the level of the 10--12th passage a stationary noncytocidal type of persistent infection was established. A low level of the infectious virus produced by the persistently infected cells was observed; the number of cells synthesizing the virus-specific antigen detectable by immunofluorescence was high. Persistently infected cells were resistant to the infection with the homologous virus and sensitive to superinfection with heterologous viruses. The persisting virus had marked interfering activity. The possibility of participation of defective interfering particles and endogenous oncornavirus in the maintenance of the persistent infection is discussed.

Animals↗